Location: Human Nutrition Research Center on Aging
Title: Effect of vitamin D supplementation on progression of knee pain and cartilage volume loss in patients with symptomatic osteoarthritis: a randomized controlled trial Authors
|Mcalindon, Timothy -|
|Lavalley, Michael -|
|Schneider, Erica -|
|Nuite, Melynn -|
|Price, Lori Lyn -|
|Lo, Grace -|
|Dawson-Hughes, Bess -|
Submitted to: Journal of the American Medical Association
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 15, 2012
Publication Date: January 9, 2013
Citation: Mcalindon, T., Lavalley, M., Schneider, E., Nuite, M., Price, L., Lo, G., Dawson-Hughes, B. 2013. Effect of vitamin D supplementation on progression of knee pain and cartilage volume loss in patients with symptomatic osteoarthritis: a randomized controlled trial. Journal of the American Medical Association. 309(2):155-162. Interpretive Summary: Knee osteoarthritis (OA) is a common disorder for which the only effective therapy is surgery. Medical therapy is urgently needed. Several observational studies have suggested that vitamin D may protect against the progression of OA. To evaluate this further, we conducted a randomized, placebo-controlled, double-blind, clinical trial of 146 participants with symptomatic knee OA, testing a 2-year vitamin D intervention (2000 International Units per day). Primary outcomes were knee pain severity and cartilage volume loss. The participants had a mean age of 62 yrs and 60% were women. The completion rate was 85%. Knee pain decreased modestly in both groups with no significant group differences at any time point. Similarly, cartilage volume decreased by the same extent in both groups. We conclude that vitamin D supplementation over two years does not influence progression of knee OA.
Technical Abstract: Knee osteoarthritis (OA), a disorder of cartilage and periarticular bone, is a public health problem without effective medical treatments. Some studies have suggested that vitamin D may protect against structural progression. A 2-year randomized, placebo-controlled, double-blind, clinical trial involving 146 participants with symptomatic knee OA (mean age, 62.4 years [SD, 8.5]; 57 women [61%], 115 white race [79%]). Patients were enrolled at Tufts Medical Center in Boston between March 2006 and June 2009. Participants were randomized to receive either placebo or oral cholecalciferol, 2000 IU/d, with dose escalation to elevate serum levels to more than 36 ng/mL. Primary outcomes were knee pain severity (Western Ontario and McMaster Universities [WOMAC] pain scale, 0-20: 0, no pain; 20, extreme pain), and cartilage volume loss measured by magnetic resonance imaging. Secondary end points included physical function, knee function (WOMAC function scale, 0-68: 0, no difficulty; 68, extreme difficulty), cartilage thickness, bone marrow lesions, and radiographic joint space width. Eighty-five percent of the participants completed the study. Serum 25-hydroxyvitamin D levels increased by a mean 16.1 ng/mL (95% CI, 13.7 to 18.6) in the treatment group and by a mean 2.1 mg/mL (95% CI, 0.5 to 3.7) (P < .001) in the placebo group. Baseline knee pain was slightly worse in the treatment group (mean, 6.9; 95% CI, 6.0 to 7.7) than in the placebo group (mean, 5.8; 95% CI, 5.0 to 6.6) (P = .08). Baseline knee function was significantly worse in the treatment group (mean, 22.7; 95% CI, 19.8 to 25.6) than in the placebo group (mean, 18.5; 95% CI, 15.8 to 21.2) (P = .04). Knee pain decreased in both groups by a mean -2.31 (95% CI, -3.24 to -1.38) in the treatment group and -1.46 (95% CI, -2.33 to -0.60) in the placebo group, with no significant differences at any time. The percentage of cartilage volume decreased by the same extent in both groups (mean, -4.30; 95% CI, -5.48 to -3.12 vs mean, -4.25; 95% CI, -6.12 to -2.39) (P = .96). There were no differences in any of the secondary clinical end points. Vitamin D supplementation for 2 years at a dose sufficient to elevate 25-hydroxyvitamin D plasma levels to higher than 36 ng/mL, when compared with placebo, did not reduce knee pain or cartilage volume loss in patients with symptomatic knee OA.